CN112353944A - Anticancer combined medicine composition containing compound F-B - Google Patents
Anticancer combined medicine composition containing compound F-B Download PDFInfo
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- A61K31/704—Compounds having saccharide radicals attached to non-saccharide compounds by glycosidic linkages attached to a carbocyclic compound, e.g. phloridzin attached to a condensed carbocyclic ring system, e.g. sennosides, thiocolchicosides, escin, daunorubicin
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Abstract
The present invention provides an anticancer combination composition comprising compound F-B, which comprises an anticancer drug having cardiotoxicity and compound F-B. The compound F-B in the composition can inhibit the myocardial fibrosis process caused by the effect of an anti-cancer medicament and inhibit the proliferation of myocardial extracellular matrix through tests; meanwhile, the compound F-B also has good cardiotoxicity resistance and can be used for preparing products for preventing and/or treating cardiac injury caused by cardiotoxic substances; the flavonoid compound F-B and the anthracycline anticancer drug with cardiotoxicity are combined to prepare the preparation, so that the cardiotoxicity of the anthracycline anticancer drug can be reduced in the treatment process of the drug with toxic side effects on the heart.
Description
Technical Field
The invention relates to the field of medical application of flavonoid compounds, in particular to an anticancer combined medicine composition containing a compound F-B.
Background
With the improvement of cancer diagnosis and treatment technology, chemotherapy has become the main adjuvant therapy for cancer. Anthracycline chemotherapeutic drugs such as adriamycin are important broad-spectrum antitumor drugs and can treat more types of tumor diseases, and chemotherapy by using the anthracycline chemotherapeutic drugs is one of the most effective and widely applied anticancer therapies at present, and can be used for treating cancers such as leukemia, lymphoma, breast cancer, uterine cancer, ovarian cancer, lung cancer and the like. The action mechanism is mainly that the anthracene ring planar structure of the molecule is inserted into the double-stranded structure of the DNA molecule, the function of the DNA is influenced, the DNA replication and the RNA transcription are inhibited, thereby the proliferation of the tumor is inhibited, and the anthracene ring planar structure is a cell cycle non-specific medicament.
The chemotherapy drugs usually have toxic and side effects such as bone marrow suppression, nausea, vomiting, stomatitis, alopecia, high fever, bleeding symptoms, phlebitis, skin pigmentation and the like, the anthracycline chemotherapy drugs also have dose-dependent cardiotoxicity besides the side effects, various arrhythmia is shown, myocardial necrosis and even congestive heart failure can occur when the accumulated dose is large, and the physical condition of a patient is seriously influenced. For this reason, efforts have been made to find effective means for reducing such toxicity, but no ideal solution has been found to date
Therefore, it is of great significance to develop anticancer drugs with lower cardiotoxicity and less damage to the heart.
Disclosure of Invention
The invention mainly solves the technical problem of providing an anticancer combined medicine composition comprising a compound F-B, and the composition has the effect of relieving heart damage caused by cardiotoxic substances.
In order to solve the technical problems, the invention provides the following technical scheme:
the invention provides an anticancer combined drug composition, which comprises an anticancer drug with cardiotoxicity and a compound F-B, wherein the structural formula of the compound F-B is as follows:
in a specific embodiment of the present invention, the anticancer drug having cardiotoxicity is an anthracycline drug.
Further, the anthracycline drug comprises one or more of doxorubicin, daunorubicin, aclarubicin, epirubicin, pirarubicin, idarubicin, and mitoxantrone.
In a specific embodiment of the invention, the anthracycline is doxorubicin.
In a specific embodiment of the present invention, in the composition for daily administration, the anticancer drug having cardiotoxicity: the mass ratio of the compound F-B is 1: 1-50, preferably 1:1 to 20, more preferably 1: 5-15, preferably 1: 10.
In a specific embodiment of the present invention, the anticancer drug having cardiotoxicity: the dosage ratio of the compound F-B is 2.5: 0.1-160, preferably 2.5: 1-80, preferably 2.5: 1-40, and more preferably 2.5: 10.
The invention also provides a product comprising the composition.
In a particular embodiment of the invention, the product further comprises pharmaceutically acceptable excipients.
Further, the pharmaceutically acceptable auxiliary materials are selected from one or more of fillers, lubricants, dispersing agents, wetting agents, adhesives, buffering agents, solubilizing agents, antioxidants, bacteriostats, emulsifying agents, disintegrating agents, chelating agents and osmotic pressure regulators.
Further, the product is in a dosage form selected from the group consisting of tablets, granules, capsules, suppositories, pills, solutions, and suspensions.
The composition provided by the invention is used for preparing a medicament for treating cancer.
In a particular embodiment of the invention, the cancer is selected from leukemia, lymphoma, breast cancer, uterine cancer, ovarian cancer or lung cancer.
The combined medicine composition can be prepared into a single compound preparation by mixing the compound F-B and the anthracycline, or can be prepared into two preparations by respectively preparing the compound F-B and the anthracycline, such as tablets, capsules or injection which are respectively prepared and then combined. When prepared separately in two formulations, the two formulations of compound F-B and the anthracycline can be administered simultaneously or independently. The number and sequence of administration of the two formulations for independent administration are not limited, and for example, the compound F-B formulation may be administered first, followed by a time interval before the anthracycline formulation; or administering an anthracycline formulation first, followed by a time interval, and then administering a compound F-B formulation; or administration of an anthracycline formulation first, followed by a time interval followed by administration of a compound F-B formulation, and the like.
The invention has the following beneficial effects:
experiments prove that the composition can reduce the ratio of heart to body weight of mice with damaged heart caused by single use of Doxorubicin (DOX) and reduce the content of hydroxyproline in heart tissues, and the compound F-B can inhibit the myocardial fibrosis process caused by the action of anthracyclines and inhibit the proliferation of myocardial extracellular matrix; meanwhile, compared with a test group using doxorubicin alone, the composition has lower expression levels of p-JNK and cleared-Caspase-3 in a myocardial apoptosis model, and shows that apoptosis in the test group of the composition is inhibited to a certain degree. The compound F-B can reduce the side effect of cardiotoxicity caused by the medicine when used together with the anticancer medicine with cardiotoxicity, and the pharmaceutical composition can reduce the cardiac injury caused by taking the anticancer medicine with cardiotoxicity in the treatment process, thereby having wide clinical application prospect.
Drawings
FIG. 1 shows the toxic effect of flavonoids on H9c2 cardiomyocytes.
FIG. 2 is a graph showing the effect of flavonoids on DOX-induced H9c2 cardiocytotoxicity.
FIG. 3 shows the effect of flavonoids on DOX-induced activation of Caspase-3 in H9c2 cardiomyocytes.
FIG. 4 shows the effect of flavonoids on DOX-induced p-JNK/JNK in H9c2 cardiomyocytes.
Wherein, in fig. 3 and 4, # P <0.05, # P <0.01, # P < 0.001; p <0.05, P <0.01, P <0.001 compared to the DOX model group; mean ± SD, n ═ 3.
Detailed Description
The technical solutions of the present invention are described clearly and completely below, and it is obvious that the described embodiments are some, not all embodiments of the present invention. All other embodiments, which can be made by those skilled in the art without any inventive work, based on the embodiments of the present invention, belong to the scope of the present invention.
The experimental methods in the examples of the present invention were all conventional methods unless otherwise specified, and the test materials used were all purchased from conventional biochemical reagents, and the data referred to in the examples were all average values.
The chemical structural formula of F-A is as follows:
the chemical structural formula of F-B is as follows:
the chemical structural formula of F-C is:
EXAMPLE 1 therapeutic Effect of Compounds F-B on Doxorubicin-induced myocardial toxicity
Rabbit test method for doxorubicin-induced cardiomyopathy (this experiment complies with relevant ethical regulations):
(1) the test was carried out with rabbits of both genders having an initial body weight of 2.3 ± 0.2kg, as untreated animals (control animals, n ═ 8) in group a, doxorubicin-treated animals (+ test substance replaced with placebo, n ═ 8) in group b, doxorubicin-and test substance-treated animals (n ═ 8) in group C, flavonoids F-A, F-B, F-C, and C1, C2, and C3, respectively.
(2) Groups b and c were administered doxorubicin 2 times per week intravenously at 1mg/kg for 4 weeks, and group c was administered orally with the test substance 20mg/kg body weight per day, starting on the first day of doxorubicin treatment, while feeding the diet.
(3) After 4 weeks, the hearts were isolated and weighed, and the hydroxyproline content in the heart tissue (determined by liquid chromatography-mass spectrometry/mass spectrometry based on the determination of L-hydroxyproline in SN/T3929-.
TABLE 1 Effect of Flavonoids of formula I on Heart recession and Change in rabbits
Note:***: p is less than 0.001, compared with the group a;+: p <0.05, compared to group b.
An increase in the ratio of heart tissue to body weight and hydroxyproline content in heart tissue compared to normal values indicates a decline and change in the heart.
The test results are shown in table 1, and the statistical values of the heart to body weight ratio of the group c of test substance animals (group c1, group c2, group c 3) were significantly reduced in terms of heart to body weight ratio compared to the group b of doxorubicin-treated animals, and reached a level that was not significantly different from that of the group a of untreated control animals; group b significantly increased the heart to body weight ratio compared to group a, and reached a very significant level. In terms of hydroxyproline content, the concentration of hydroxyproline in the group c is obviously lower than that of hydroxyproline in the group b, and an extremely significant level is reached, which indicates that the fibrosis degree of the hydroxyproline is inhibited to a certain extent; the hydroxyproline concentration in group b was significantly higher than in group a, indicating that doxorubicin induced fibrosis in the heart tissue.
Therefore, by administering the test substance, the flavonoid compound can obviously reduce the change process of extracellular myocardial matrix, inhibit the proliferation of myocardial extracellular matrix and has the effect of preventing and/or treating the myocardial toxicity.
EXAMPLE 2 therapeutic Effect of Compounds F-B on Doxorubicin-induced myocardial toxicity
Inhibition of cardiomyocyte apoptosis in the H9c2 cardiotoxicity model:
(1) after H9C2 cells are incubated for 24H by using different concentrations of flavonoids F-A, F-B, F-C, the toxicity effect of the flavonoids on the myocardial cells is evaluated by adopting an MTT colorimetric method, the H9C2 cells are incubated for 1H by using the flavonoids in advance, then 2.5 mu M DOX is added for culturing for 24H, the MTT colorimetric method is adopted to screen the apoptosis activity of the flavonoids on the Doxorubicin (DOX) induced myocardial cells, and the optimal action concentration range is determined.
(2) Treating different tested sea buckthorn flavonoids with H9c2 cardiomyocytes for 1H, treating with 2.5 mu M DOX for 24H to extract protein, cracking, scraping, collecting cell lysate, centrifuging at 12000g for 15min, collecting supernatant, discarding precipitate, storing at-80 ℃, and quantifying the protein by using a BCA method for later use; SDS-PAGE (Step1, 80V, 30 min; Step2,120V,180min), 5% gel concentrate; transferring the membrane and PVDF membrane for 30min and 80 mA; sealing and hybridizing, sealing with 5% skimmed milk powder for 1h, incubating overnight with primary antibody, and incubating with secondary antibody at room temperature for 1-2 h with gentle shaking; and developing by using an ECL reagent, and observing the expression conditions of Caspase-3 and p-JNK/JNK proteins in the cells by using a gel imaging system.
The test result is shown in fig. 1, the flavonoid compound has no statistical difference (0.1-40 μ M) compared with the Con group in a certain concentration range, but has a significant difference compared with the Con group when reaching 80 μ M, which indicates that exceeding the concentration may have a certain toxic effect on the activity of H9c2 cells.
The results of fig. 2 show that the flavonoid group with different concentration ranges and the DOX model group both show the inhibition of the DOX-induced myocardial cytotoxicity and show certain concentration dependence, and the concentration is within the range of 5-80 μ M and has significant difference or extremely significant difference compared with the model group.
FIG. 3 shows that the DOX model group can greatly increase the expression level of cleared-Caspase-3 compared with the Con group, and the low, medium and high dose groups (10. mu.M, 20. mu.M and 40. mu.M) of flavonoids can reduce the rising level of cleared-Caspase-3 caused by DOX to different degrees compared with the DOX model group, and a remarkable concentration dependence relationship exists; as shown in fig. 4, the DOX model group was able to significantly increase p-JNK expression levels compared to the Con group. There is no statistical difference in p-JNK expression levels between the flavonoid low dose group (10 μ M) and the DOX model group, but the medium dose group (20 μ M) and the high dose group (40 μ M) have very significant difference and have obvious concentration dependence relationship. Therefore, the flavonoid compound can reduce the expression level of p-JNK in a DOX-induced myocardial cell apoptosis model, and the analysis of the influence of the flavonoid compound on the expression level of cleared-Caspase-3 shows that the flavonoid compound provided by the invention can reduce the expression level of p-JNK/cleared-Caspase-3 to inhibit DOX-induced myocardial cell apoptosis and relieve the toxic effect of myocardial cells.
Therefore, by administering the test substance, the flavonoid compound can inhibit the apoptosis induced by the cardiotoxicity effect by down-regulating the expression level of p-JNK/cleared-Caspase-3, thereby realizing the prevention and/or treatment effect.
In conclusion, the flavonoid compound disclosed by the invention has the effects of inhibiting myocardial fibrosis, myocardial extracellular matrix hyperplasia and myocardial toxicity induced apoptosis and relieving myocardial cytotoxicity, and can be used for preparing a medicine for preventing and/or treating heart injury.
The flavonoid compound is suitable for being used as a medicine for mammals, particularly human bodies, and is used for preventing and/or treating damage influence caused by cardiotoxic dose of medicines and heart damage conditions caused by other chemical substances, particularly decline and change of hearts, such as cardiotoxicity, myocardial fibrosis and the like of anthracycline anticancer medicines. The flavonoid compounds of the invention can be used as medicaments, in particular as adjuvant treatment in the treatment process of anticancer medicaments with toxic side effects on the heart. The amount used may vary and may vary depending on the type of treatment, the substance used and the form of administration, whether intravenous, oral, etc.
Example 3 tablet containing flavonoid Compound
Each tablet was produced with the following ingredients:
mixing the above materials according to the above dosage, granulating, mixing, and tabletting to obtain 250mg tablet.
Example 4 injection solution containing flavonoid Compound
Injections were produced per 1ml with the following composition:
the above solid matter was dissolved in purified water, and the solution was aseptically filled in 1ml ampules.
The above description is only an embodiment of the present invention, and not intended to limit the scope of the present invention, and all changes in equivalent flow or equivalent structure, which are made by using the description of the present invention and are directly or indirectly applied to other related technical fields should be covered by the scope of the present invention.
Claims (10)
1. An anticancer combination composition, which is characterized by comprising an anticancer drug with cardiotoxicity and a compound F-B, wherein the structural formula of the compound F-B is as follows:
2. the composition of claim 1, wherein the cardiotoxic anticancer agent is an anthracycline.
3. The composition according to claim 2, wherein the anthracycline includes one or more of doxorubicin, daunorubicin, aclarubicin, epirubicin, pirarubicin, idarubicin, mitoxantrone.
4. The composition of claim 3, wherein the anthracycline is doxorubicin.
5. The composition according to any one of claims 1 to 4, wherein the anticancer drug with cardiotoxicity: the mass ratio of the compound F-B is 1: 1-50, preferably 1:1 to 20, more preferably 1: 5-15, preferably 1: 10.
6. The composition according to any one of claims 1 to 4, wherein the cardiotoxic anticancer agent: the dosage ratio of the compound F-B is 2.5: 0.1-160, preferably 2.5: 1-80, preferably 2.5: 1-40, and more preferably 2.5: 10.
7. A product comprising the composition of any one of claims 1 to 6.
8. The product of claim 7, further comprising a pharmaceutically acceptable excipient.
9. Use of a composition according to any one of claims 1 to 6 in the manufacture of a medicament for the treatment of cancer.
10. Use according to claim 9, wherein the cancer is selected from leukemia, lymphoma, breast cancer, uterine cancer, ovarian cancer or lung cancer.
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Citations (9)
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|---|---|---|---|---|
| CN102274236A (en) * | 2010-06-13 | 2011-12-14 | 上海市第六人民医院 | Drug for prevention and treatment of cardiotoxicity induced by anthracycline antibiotics, and application thereof |
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| CN111635445A (en) * | 2020-06-29 | 2020-09-08 | 中国科学院西北高原生物研究所 | Novel flavonoid compound Hip A and application thereof |
| CN111635441A (en) * | 2020-06-29 | 2020-09-08 | 中国科学院西北高原生物研究所 | New flavonoid Hyd and application thereof |
| CN111704642A (en) * | 2020-06-29 | 2020-09-25 | 中国科学院西北高原生物研究所 | Novel flavonoid compounds Hip B and Hip C and application thereof |
| CN111714508A (en) * | 2020-06-29 | 2020-09-29 | 中国科学院西北高原生物研究所 | Application of neoflavonoid Hip B and Hip C |
-
2020
- 2020-11-23 CN CN202011325330.XA patent/CN112353944A/en active Pending
Patent Citations (9)
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